Local immune surveillance appears to be deficient in women with endometriosis and immune cells seem to paradoxically favor ectopic endometrial cell growth via different mechanisms that include secretion of inflammatory, angiogenic and growth mediators such as monocyte chemotactic protein 1 (MCP1), macrophage migration inhibitory factor (MIF), interleukin 1 (IL1), IL8, and vascular endothelial cell growth factor (VEGF) [3]. Here, CCL2 is linked to endometriosis.